Stomach function and architecture vary widely between mammalian species, to accommodate a wide variety of habitats and diets. Consequently, non-human models of gastric development and disease have significant limitations. For example, the bacterium Helicobacter Pylori infects 50% of the world's population, with 10% developing peptic ulcer disease and 1-2%1-3 developing gastric cancer. Gastric diseases, including peptic ulcer disease and gastric cancer, affect 10% of the world's population and are largely due to chronic H. pylori infection. Current models of H. pylori-induced disease rely upon animal models that do not exhibit the same pathophysiological features as the human response to infection4, and gastric cell lines lack the cellular and architectural complexity of the gastric epithelium in vivo. Thus there is no adequate model to study the effects of H. pylori infection as it occurs in humans. While recent advances using adult gastric stem cells allow for growth of rodent gastric epithelium in vitro5, obtaining these cells from human patients would require surgery. Moreover, such a method could not be used to model embryonic development of the human stomach or stromal-epithelial interactions. Species differences in embryonic development and architecture of the adult stomach make murine models suboptimal for the study of organogenesis and pathogenesis of this organ. Thus, there is a need for robust in vitro systems for elucidating the mechanisms underlying human stomach development and disease and for the identification of novel treatments useful for human treatment of such diseases.
What is needed in the art are methods and systems for accurately controlling the destination of a precursor cell such as a human pluripotent stem cell, in order to create the specific type of tissue or organism desired, in particular, gastric tissues that can be used for one or more of the aforementioned purposes.